eMedicine Specialties > Cardiology > Arrhythmias

Electrical Alternans

Eric Gorgon Shaw, MD, FACEP, FAAEM, Staff Physician, Department of Emergency Medicine, Lewis County General Hospital
Michael R Gold, MD, PhD, Director, Professor, Division of Cardiology, Medical University of South Carolina; Amal Mattu, MD, FACEP, FAAEM, Program Director, Emergency Medicine Residency, Co-Director, Emergency Medicine/Internal Medicine Combined Residency Program, Department of Surgery, Division of Emergency Medicine, University of Maryland School of Medicine

Updated: Aug 26, 2008

Introduction

Background

Electrical alternans is a broad term that describes alternate-beat variation in the direction, amplitude, and duration of any component of the ECG waveform (ie, P, PR, QRS, R-R, ST, T, U). It was first recognized by Hearing in 1909 and further characterized by Sir Thomas Lewis in 1910 as occurring "either when the heart muscle is normal but the heart rate is very fast or when there is serious heart disease and the rate is normal." Kalter and Schwartz first identified electrical alternans on surface ECG in 1948.¹⁶ Electrical alternans must be distinguished from mechanical alternans (eg, pulsus alternans), although both may coexist.

Pathophysiology

The pathophysiologic mechanisms that cause electrical alternans can be divided into 3 categories: (1) repolarization alternans (ST, T, U alternans), (2) conduction and refractoriness alternans (P, PR, QRS alternans), and (3) alternans due to cardiac motion. True electrical alternans is a repolarization or conduction abnormality of the Purkinje fibers or myocardium. Electrical alternans due to cardiac motion is effectively artifact, as the heart swings in relation to the chest wall and electrodes, with a period twice that of the heart rate.

Repolarization alternans can be further subclassified as T-wave alternans and ST-segment alternans. T-wave alternans is associated with rapid changes in heart rate or prolongation of the QT interval. A long QT interval is associated with polymorphic ventricular tachycardia (ie, torsade de pointes); therefore, T-wave alternans is a possible precursor to torsade de pointes.

T-wave alternans has been reported with congenital long QT syndrome¹ , electrolyte imbalances (eg, hypocalcemia, hypokalemia, hypomagnesemia), treatment with quinidine or amiodarone² , hypertrophic cardiomyopathy, alcoholic cardiomyopathy, congestive heart failure, and acute pulmonary embolism. T-wave alternans has also been reported following cardiac resuscitation. Most importantly, the presence of T-wave alternans can be used as a predictor of ventricular tachyarrhythmic events, such as sudden cardiac death³ , sustained ventricular tachycardia, ventricular fibrillation, implantable cardioverter defibrillator (ICD) therapy for ventricular tachyarrhythmia, and cardiac arrest.

ST-segment alternans describes alternating levels of ST elevation, usually in the presence of myocardial ischemia. It has been reported with vasospastic angina pectoris, acute myocardial infarction, nonvasospastic angina pectoris, during exercise tests, during percutaneous transluminal coronary angioplasty (PTCA), and after subarachnoid hemorrhage⁴ . ST alternans during acute ischemia has been associated with appearance of ventricular arrhythmia, including ventricular tachycardia and ventricular fibrillation.

Conduction alternans is an alternation of impulse propagation along any of the anatomic structures involved in conveyance of electrical impulse and is usually precipitated by changes in heart rate or input from nervous, humoral, or pharmacologic components. Conduction alternans may be seen in the setting of myocardial ischemia, atrial fibrillation, Wolff-Parkinson-White syndrome, rheumatic heart disease, acute pulmonary embolism, myocardial contusion, and left ventricular dysfunction. It may manifest on the surface ECG as alternation of the P wave, QRS complex, PR interval, R-R interval, or any combination of these. QRS alternans during narrow complex tachycardia has been suggested as a marker for orthodromic atrioventricular (AV) reentrant tachycardia using an accessory pathway as a retrograde limb.

Electrical alternans associated with cardiac motion is due to alternation in the position of the heart with relation to recording electrodes. The most common underlying disorder is an enlarged pericardial sac; however, not all pericardial effusions cause electrical alternans. The presence of pericardial disease and total electrical alternans (P, QRS, and T wave) frequently suggests cardiac tamponade, but total electrical alternans is seen in only 5-10% of patients with cardiac tamponade. Heart movement in patients with hypertrophic cardiomyopathy also may result in electrical alternans of this type.

Frequency

United States

Incidence of electrical alternans is estimated to be about 1-6 of 10,000 ECGs. Overall, QRS alternans is the most common type. ST alternans incidence has been reported as 5–7.7% of patients during PTCA using intracoronary ECG recordings. T-wave alternans was observed in 45% of patients with congenital long QT syndrome after examining 24-hour Holter monitors.

Mortality/Morbidity

The finding of electrical alternans does not alter the morbidity and mortality rates of the underlying cause or association.

Clinical

History

The presence of electrical alternans has no clinical manifestations outside those present from the underlying cause or association. A search for the underlying cause of electrical alternans is warranted. For example, the patient with ST-T alternans may complain of chest pain, shortness of breath, or profuse sweating caused by myocardial ischemia. The patient with QRS alternans may complain of syncope resulting from underlying hypertrophic cardiomyopathy.

Physical

Electrical alternans does not result in physical findings separate from the underlying cause of the alternans. A physical examination, searching for the underlying cause, is necessary. This may reveal, for example, jugular venous distention and hypotension from cardiac tamponade. Making the distinction between electrical alternans and mechanical alternans is important. Mechanical alternans may have physical findings (eg, pulsus alternans).

Causes

• The reported causes or associations of electrical alternans have been mentioned already and are relisted here for convenience.
• Repolarization (ST–T alternans)
  • Vasospastic angina pectoris
  • Acute myocardial infarction
  • Nonvasospastic angina pectoris
  • Congenital long QT syndrome
  • Electrolyte imbalances, such as hypocalcemia, hypokalemia, and hypomagnesemia
  • Treatment with quinidine
  • Treatment with amiodarone
  • Hypertrophic cardiomyopathy
  • Alcoholic cardiomyopathy
  • Congestive heart failure (See Medscape's Heart Failure Resource Center.)
  • Acute pulmonary embolism
  • Following cardiac resuscitation
  • During exercise tests
  • Acute mental stress
  • During PTCA
  • After subarachnoid hemorrhage
• Conduction (QRS alternans)
  • Myocardial ischemia
  • Atrial fibrillation
  • Wolff-Parkinson-White syndrome
  • Rheumatic heart disease
  • Acute pulmonary embolism
  • Myocardial contusion
  • Left ventricular dysfunction
• Cardiac motion
  • Large pericardial effusion
  • Hypertrophic cardiomyopathy

Differential Diagnoses

Workup

Laboratory Studies

Direct laboratory investigations toward discovery of the primary underlying etiology of electrical alternans. Based on other clinical information, appropriate lab studies include cardiac enzymes for myocardial ischemia and infarction as well as serum calcium, potassium, and magnesium if electrolyte abnormalities are suspected. In the setting of a large pericardial effusion, laboratory studies searching for a malignancy may be warranted.

Imaging Studies

• Chest radiography
  • Chest radiograph may reveal an enlarged cardiac silhouette, possibly indicating cardiomyopathy or large pericardial effusion.
  • Evidence of the Westermark sign or Hampton hump may suggest pulmonary embolism as the cause of electrical alternans.
• Echocardiography
  • Echocardiography should be performed on those patients with total electrical alternans (P, QRS, and T wave) to evaluate for pericardial effusion.
  • Echocardiography is also necessary for evaluation of patients with hypertrophic cardiomyopathy, alcoholic cardiomyopathy, or congestive heart failure.

Other Tests

• Electrocardiogram
  • ECG is the main study through which electrical alternans is discovered. Any or all components of the electrical waveforms may exhibit alternans (see Media files 1-2).
  • High-resolution ECG with spectral analysis can detect alternans in the microvolt range of amplitude. This detailed study is appropriate when searching for T-wave alternans as a predictor of ventricular tachyarrhythmia events.⁵
  • Routine ambulatory ECG monitoring of T-wave alternans, using dynamic, nonspectral, modified moving average analysis, may be helpful for risk stratification for arrhythmias.
  • T-wave alternans may be seen best in lead V ₂ .
  • T-wave alternans can be detected by use of implantable cardioverter-defibrillators (ICDs).⁶

Procedures

• Electrical alternans due to a large pericardial effusion should resolve completely after the effusion is drained. Pericardiocentesis must be performed emergently in the setting of cardiac tamponade.
• In selected cases, cardiac catheterization may be indicated to further evaluate those patients with suspected vasospastic or nonvasospastic angina pectoris.

Treatment

Medical Care

Direct treatment toward correction of the underlying cause of electrical alternans. For example, myocardial infarction should be treated using standard measures (eg, consider thrombolytic administration or PTCA). Long QT syndrome may be treated with removal of offending drugs or correction of metabolic abnormalities.

Surgical Care

Most diseases that cause true electrical alternans do not require surgical treatment. Pulmonary embolectomy may be required for unresolved large pulmonary emboli. Left-sided cervicothoracic sympathetic ganglionectomy may be required for patients with congenital long QT syndrome who continue to have episodes of syncope despite drug therapy. Recurrent pericardial effusions may benefit from pericardiectomy.

Consultations

Cardiology consultation is usually indicated.

Diet

No specific dietary restrictions are required aside from those required for the underlying cause (eg, salt restriction for congestive heart failure).

Activity

No specific activity restrictions are required aside from those required for the underlying cause (eg, avoidance of stress and strenuous exercise for patients with congenital long QT syndrome in order to prevent an arrhythmia in susceptible patients).

Medication

No medications are specifically indicated for correction of electrical alternans. Biomedical research on canines may result in future pharmacotherapy for T-wave alternans. Please refer to the corresponding articles on underlying diseases for specific medications.

Follow-up

Complications

No known complications of electrical alternans exist. All complications are due to the underlying disease process.

Prognosis

The finding of electrical alternans does not change the prognosis of the underlying disease process.

Miscellaneous

Medicolegal Pitfalls

• Failure to recognize electrical alternans on ECG, resulting in detrimental progression of the underlying disease process
• Delay of emergent pericardiocentesis for correction of cardiac tamponade due to failure of recognition of electrical alternans

Multimedia

Media file 1: Typical alternate-beat QRS electrical alternans. Note that QRS voltage is low.

Media file 2: Supraventricular tachycardia with alternans. Note the phasic nature to the QRS morphology, particularly in the rhythm strip in V1.

References

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6. Paz O, Zhou X, Gillberg J, Tseng HJ, Gang E, Swerdlow C. Detection of T-wave alternans using an implantable cardioverter-defibrillator. Heart Rhythm. Jul 2006;3(7):791-7. [Medline].

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Keywords

mechanical alternans, pulsus alternans, repolarization alternans, conduction and refractoriness alternans, alternans due to cardiac motion, repolarization or conduction abnormality of the Purkinje fibers or myocardium, vasospastic angina pectoris, acute myocardial infarction, nonvasospastic angina pectoris, congenital long QT syndrome, hypocalcemia, hypokalemia, hypomagnesemia, hypertrophic cardiomyopathy, alcoholic cardiomyopathy, congestive heart failure, acute pulmonary embolism, cardiac resuscitation, myocardial ischemia, atrial fibrillation, Wolff-Parkinson-White syndrome, rheumatic heart disease, acute pulmonary embolism, myocardial contusion, left ventricular dysfunction, large pericardial effusion, hypertrophic cardiomyopathy

Contributor Information and Disclosures

Author

Eric Gorgon Shaw, MD, FACEP, FAAEM, Staff Physician, Department of Emergency Medicine, Lewis County General Hospital
Eric Gorgon Shaw, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

Michael R Gold, MD, PhD, Director, Professor, Division of Cardiology, Medical University of South Carolina
Michael R Gold, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Chest Physicians, and American Heart Association
Disclosure: Nothing to disclose.

Amal Mattu, MD, FACEP, FAAEM, Program Director, Emergency Medicine Residency, Co-Director, Emergency Medicine/Internal Medicine Combined Residency Program, Department of Surgery, Division of Emergency Medicine, University of Maryland School of Medicine
Amal Mattu, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Robert E Fowles, MD, Clinical Professor of Medicine, University of Utah College of Medicine; Consulting Staff, Intermountain Medical Center and LDS Hospital; Director and Consulting Staff, Department of Cardiology, Salt Lake Clinic
Robert E Fowles, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Steven J Compton, MD, FACC, FACP, Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals
Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, and Heart Rhythm Society
Disclosure: Nothing to disclose.

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

J Paul Mounsey, MD, PhD, MRCP, Professor of Medicine, Director, Cardiac Electrophysiology Service, Division of Cardiology, University of North Carolina
J Paul Mounsey, MD, PhD, MRCP is a member of the following medical societies: American College of Cardiology, American Heart Association, Heart Rhythm Society, and Royal College of Physicians of the United Kingdom
Disclosure: Medtronic Honoraria Speaking and teaching; St Jude Honoraria Speaking and teaching; Boston Scientific Honoraria Speaking and teaching

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